The Connective IssueThe Fascia Institute & Treatment Center Journal
A weekly report from the studio floor of fascia medicine — where movement, recovery, and staying in the show meet.
The performance is Friday. The treatment has to be today.
We are changing the theme this week. Thirteen issues of football, and now the sport where the margin for downtime is zero.
A dancer cannot take two days off to be sore. Neither can a musician on tour, a surgeon on call, a nurse working doubles, or anyone in the back half of a season. This is a category of patient we see constantly and almost nobody designs care around: people who cannot stop performing while they get better.
That constraint changes what good treatment looks like. It rules out anything that trades tomorrow for today. And it puts a premium on two things: therapies that leave you able to work immediately, and medications that treat pain without dulling you.
So this week, both. Our cover story is low-dose naltrexone — a very small dose of a very old drug that has become one of the more useful tools we have for chronic pain, and one of the most misunderstood. I have just published a full guide to it on our site; this issue is the honest short version, including the trial that did not work.
Then TECAR, and why it has become the in-season athlete’s therapy — including, apparently, Shakira’s. No downtime, no soreness tax, and you can go straight from the table to rehearsal.
Also: OxeFit assessments are still free all month, and the calendar is going faster than either city expected. And a spotlight I have been looking forward to — Irina Parau, who runs our Beverly Hills clinic and moved across the country to do it.
Places, please. Let’s begin.
In This Issue
- A Very Small Dose of a Very Old Drug Center Stage
- Shakira Does TECAR. So Do Our In-Season Athletes. Company Class
- Spotlight: Irina Parau, Clinical Director, FIT LA Principal
- OxeFit Is Free All September Encore
- The Single-Leg Heel Rise At the Barre
A very small dose of a very old drug.
Naltrexone has been on the market since 1984. At somewhere between a tenth and a thirtieth of its approved dose it stops behaving like an addiction medicine and appears to start behaving like an anti-inflammatory. That is the whole idea behind low-dose naltrexone — and it is the closest thing we have to a pain medication that does not cost you your clarity.
Here is the conversation I have most often about it. A patient has had pain for years. They have been offered anti-inflammatories that upset their stomach, gabapentinoids that made them foggy, and opioids they did not want. Someone mentions LDN. They look it up, find a wall of enthusiasm on one side and dismissiveness on the other, and arrive asking me which one is right.
Neither, exactly. I have just published a long guide to this on our site, and this is the short version.
The difference that matters most
Naltrexone is an opioid antagonist — the pharmacologic opposite of an opioid. It is in the same family as naloxone, the drug in every ambulance. It cannot produce euphoria, it is not sedating, and the FDA label states plainly that it does not lead to dependence or tolerance. It is also not a DEA-controlled substance: no monitoring database, no controlled-substance agreement, no random urine screens, no thirty-day limit, no monthly visit just to get a refill. If you have spent years being treated as a liability by the pain-management system, that changes the entire experience of being treated.
The best evidence for the clearer-head claim is a head-to-head trial. In 67 patients with painful diabetic neuropathy, LDN relieved pain about as well as amitriptyline — a standard neuropathic drug famous for grogginess — and produced 8 adverse events against amitriptyline’s 52. The most common problem on amitriptyline was somnolence. On LDN it was mild diarrhea.
What it may be doing
In long-standing pain the original injury often stops being the problem and the nervous system becomes the amplifier. Much of that amplification comes from glial cells, particularly the microglia of the brain and spinal cord, which release inflammatory signals that make neighboring pain neurons more excitable. There are two proposed explanations for what LDN does about it:
Glial quieting at TLR4
At very low concentrations naltrexone appears to act at Toll-like receptor 4, a non-opioid receptor on microglia that drives inflammatory signaling. In laboratory and animal models, blocking it reduces glial activation and reverses pain behavior — entirely separately from anything naltrexone does at opioid receptors.
Brief blockade, then rebound
Naltrexone clears fast. The theory is that a small dose briefly and partially blocks opioid receptors, and the body answers by making more of its own opioid peptides. You will see this called “endorphin rebound,” but the one human biomarker study found met-enkephalin rose while beta-endorphin did not — so opioid peptide upregulation is the more accurate name.
Now the part most websites leave out: neither mechanism has been demonstrated in a living human being. A 2026 review put it plainly — these rest on cell-culture and animal data, no human study has confirmed them with a biomarker or a scan, and much of the glial research used the mirror-image form of the molecule rather than the one patients actually take. The mechanism is plausible and biologically coherent. It is not proven, and anyone who tells you exactly how LDN works in your body has gone past the evidence.
What the evidence supports, stated honestly
Fibromyalgia is the most studied and the results are genuinely mixed. A 2013 randomized crossover trial found pain down 28.8% on LDN against 18.0% on placebo. Then the Danish trial that should temper everyone’s expectations: 99 women, the largest and best-powered study to date, pain down 1.3 points on LDN and 0.9 on placebo — a difference of 0.34 points that was not statistically significant. That was a negative trial and any honest account has to say so. Meta-analyses pooling the smaller trials do find a significant but modest benefit, and the Danish investigators have formally disputed that pooled estimate in print. Meanwhile the largest real-world review — 93 chronic-pain patients in one practice — found 53.8% reported meaningful relief, with the highest response rates in mast cell activation and arthritis-related conditions. The fair summary: a real but modest average effect, wide variation between individuals, and reasonable experts disagreeing about its size. Roughly half of patients benefit, which means roughly half do not.
And for the group that asks me about this most often, the candid version: there are no controlled trials of LDN in hEDS, hypermobility spectrum disorder, or MCAS, and none currently registered. Expert consensus guidance on pain in the Ehlers-Danlos syndromes includes LDN while describing the support for it as anecdotal. We prescribe it because the mechanism fits, the safety profile is favorable, and many of our patients report benefit — not because a trial has proven it.
Where we start, and why it is not 4.5 mg
What follows describes how this is prescribed in our clinic. It is not a protocol to follow on your own and not a recommendation that you take this drug. LDN requires a prescription, a compounding pharmacy, and a physician who knows your full medication list.
The dose you will read about online is 4.5 mg. That number comes from the trials, not from physiology, and treating it as the destination is the most common mistake made with this drug. The best dose-finding study titrated 41 patients upward in 0.1 mg steps and found effective doses scattered from 0.1 to 5.6 mg, clustering toward the low end, with no single most-common dose. The authors concluded that starting everyone at a fixed 4.5 mg may be ill-advised.
So we begin at 1.5 mg or lower and move up only if the current dose is well tolerated and the benefit has stopped improving. For patients with mast cell activation, hypermobility, POTS, or ME/CFS — or anyone with a history of reacting to medications — we start at 0.1 to 0.5 mg using a compounded liquid, which moves in increments a capsule cannot. Starting too high is the single most common reason someone concludes LDN does not work for them, when the real problem was the ramp.
It has to be compounded, because the smallest manufactured tablet is 50 mg. One caution, since people shop for this online: compounded preparations are not FDA-reviewed for quality before dispensing, and potency does vary. Where it comes from matters.
Give it time. Some patients notice something in two to four weeks; many need eight to twelve weeks at a stable dose before the picture is clear. We do not call a trial a failure early. And if a previous trial at a flat 4.5 mg failed, that is often a reason to retry it properly rather than a reason to rule it out.
If you take opioids
This is the one interaction that requires real care, and the honest answer is more nuanced than either the drug label or the internet suggests.
The familiar rule — seven to ten days opioid-free before starting — comes from the 50 mg label, a dose more than thirty times where we start. At low and ultra-low doses the published picture looks different, and in some respects opposite: adding ultra-low-dose naltrexone to oxycodone enhanced and prolonged pain relief in a randomized trial, ultra-low doses added to methadone reduced side effects, and a large Norwegian prescription cohort found opioid use fell after patients started LDN.
So being on opioids is not an automatic no. We do prescribe LDN to selected patients on stable opioid therapy — often the very patients we are helping taper — starting at 0.1 mg or less and titrating slowly. What makes that safe is the dose and the supervision. Never start it yourself while taking opioids, and tell us about all of them, including tramadol and codeine cough preparations.
Surgery and emergencies. Tell your surgeon and anesthesiologist you take naltrexone. Current anesthesia guidance is to hold it beforehand, most commonly 48 to 72 hours, because opioid pain relief may be blunted or unpredictable. Keep a note in your phone in case of an accident. This is entirely manageable with planning and a real problem only if nobody knows.
The first few weeks, and the price
Side effects are front-loaded and usually mild. Vivid dreams are the most consistent finding, running about 2.4 times placebo — most patients find them interesting, and if not, we move the dose to the morning. Then disturbed sleep, nausea (the most common reason people stop, usually fixed by taking it with food and stepping back down), and occasionally fatigue, which is more often a signal the dose is too high than too low. Some patients flare briefly in the first week or two; we hold rather than push through. Serious events have been rare across every published trial — though those trials are small and mostly twelve weeks or less, so long-term risks cannot be fully excluded.
It costs $30 to $60 a month, paid to the compounding pharmacy. Insurance essentially never covers it — which also means no prior authorization, no step therapy, no formulary tier, and no appeal letter. HSA and FSA funds generally work. The flip side is that it is genuinely out of pocket and does not count toward a deductible, and you should know that going in rather than at the counter.
And what it is not. Not a cure for anything. Not a repair for connective tissue and not a treatment for hypermobility itself. Not natural, not a supplement. Not FDA-approved for pain. Not effective for everyone. At best, it turns down the volume on a sensitized nervous system — and it works best as one part of a plan rather than as the plan.
Educational information only, not medical advice and not a treatment recommendation for any individual. LDN is an off-label, compounded use of an approved medication. If you take opioid medication of any kind, LDN must be started and supervised by a physician — never on your own. Do not start, stop, or adjust any prescription without your physician.
Shakira does TECAR. So do our in-season athletes.
Human Tecar counts Shakira among the performers who use the technology on tour. It is a good headline. The more useful part is why a touring artist would choose it over a massage.
Think about what a tour actually demands. Two hours of high-output movement in heels, a bus, a hotel, and another two hours the next night. There is no recovery week. Whatever treatment she gets has to leave her able to perform within hours.
That is the same problem a dancer has in performance season, a basketball player has in February, and a nurse has on her fourth twelve-hour shift. It is the problem TECAR happens to be good at.
What TECAR is
TECAR stands for Transfer of Energy Capacitive and Resistive. The Human Tecar system we use delivers radiofrequency current through the body at 447 kHz — other TECAR devices run at other frequencies — and it is a frequency the tissue itself completes the circuit for — meaning the energy is generated inside the tissue rather than applied to the surface of it. Two electrode types do two different jobs:
Capacitive
These electrodes concentrate the effect in soft, well-vascularized tissue — muscle, superficial fascia. This is where a heavy, overworked quadriceps or calf lives.
Resistive
These drive deeper, into tissue that carries less blood — tendon, ligament, joint capsule, scar. Achilles, patellar tendon, plantar fascia, an old ankle that never quite came back.
It can be run with or without a thermal effect. In my experience an irritated tendon in season often does better on the non-thermal setting than with heat — that is clinical preference, not a trial result.
And since I held LDN to a standard above, the same standard here: the published trials do report reduced pain and improved range of motion, but they are small, the protocols vary, follow-up is short, and a 2026 review of TECAR for tennis elbow specifically called the evidence low-certainty. The strongest data are in frozen shoulder, neck and low back pain, and knee problems. For ligament injuries it is thin to absent. It is used widely in European sports medicine, where it first earned its reputation getting injured athletes back into competition quickly.
Why we reach for it when someone has to perform
I want to be careful here, because this is a comparison of tools rather than a verdict on one of them. Manual therapy is not going anywhere in this practice, and a skilled pair of hands does things no machine does.
But deep tissue work has a cost that nobody tells you about until you have a show that night: it can leave you sore. Aggressive manual work produces its own small inflammatory response, and the twenty-four to forty-eight hours afterward can be worse before they are better. That is fine in the off-season. It is a real problem the night of a performance or the day before a game.
Two other practical advantages for the in-season body. It reaches structures that are simply too deep to treat manually — you cannot get a hand around a hip capsule. And because the dose is delivered as energy rather than pressure, treatment does not have to hurt to work, which matters for hypermobile and pain-sensitized patients who often cannot tolerate deep manual work at all.
What I would not claim: that there is a body of head-to-head trials proving TECAR outperforms massage. There is not. What does exist is a handful of add-on trials — manual therapy with TECAR against manual therapy alone — where the groups getting TECAR did somewhat better. That is suggestive, not conclusive. The rest of the case above is mechanism plus a decade of watching which patients get back on the floor faster. Take it as clinical judgment offered plainly, which is what it is.
Who we use it for
- Dancers and performers in season — treatment on a show day without paying for it on stage.
- In-season athletes — the point in the calendar when nobody can afford two days of soreness.
- Chronic tendon problems — Achilles, patellar, gluteal, plantar fascia, where depth is the whole difficulty.
- Hypermobile and pain-sensitized patients — meaningful depth of treatment without deep pressure.
- Post-injury stiffness and scar — tissue that has stopped gliding and needs to be persuaded, not forced.
Not appropriate for everyone. TECAR is generally avoided over metal implants and surgical hardware; over implanted electronics including pacemakers, defibrillators, spinal cord stimulators, and insulin or intrathecal pumps; in pregnancy; over active malignancy, active infection, or acute thrombosis; in epilepsy; in significant cardiovascular disease or impaired temperature regulation; and where sensation is significantly reduced. Tell us about all of it — we screen, but we need to know. One more, because it matters for a lot of our patients: heat can trigger mast cell degranulation and is poorly tolerated in POTS and dysautonomia. If that is you, say so, and we will use the non-thermal setting or a different tool. Educational information only, not medical advice.
She moved across the country to open our second stage.
Irina Parau · Clinical Director, The Fascia Institute LA
The medicine travels fine when you open a clinic two thousand miles away. The standard does not, unless somebody carries it. Irina carried it.
Irina Parau is the Clinical Director of FIT LA, and the honest description of her job is everything. Patient coordination. Our hypermobility clinic. Facilities. Recruiting and interviews. Referrals. Community relations. If you have been seen in Beverly Hills and it felt organized, that is her — and so is the fact that the person who saw you was the right one for what you have.
She did not get there by an easy road. Irina came to New Orleans from Romania to play Division I basketball at Tulane. Then, when we opened on the West Coast, she left the city where she had built a life and moved to Los Angeles to run a clinic in a market where she knew almost no one. Twice now she has bet on herself in an unfamiliar place. Twice it has worked.
The basketball matters more than it sounds like it should. Our patients come to us because something in their body stopped doing what it used to. Irina has been on the other side of that — the training load, the mechanics, the recovery, the pressure to be available. When a patient tells her a hip does not feel right, she is not translating. She already speaks it.
I asked her what the first six months have been like.
Taking the opportunity to be the clinical director of FIT LA was a decision I made without hesitation, and one I’ve been grateful for every day since. I’ve always embraced challenges, and launching a clinic in a new market, the Beverly Hills Golden Triangle, no less, has been both incredibly rewarding and a tremendous opportunity for growth. What strikes me most is how similar our patients are, and no matter where they come from, they all share the same story: a long journey searching for the right care and a life free from pain. Every day, we hear heartfelt testimonials from patients who’ve finally found hope and relief after so long. That’s what keeps me inspired, and I feel truly grateful to lead FIT LA.
— Irina Parau
I want to sit on one line of that. They all share the same story.
We went from New Orleans to Beverly Hills half expecting to meet a different patient. We did not. Different zip code, same file: years of appointments, a stack of normal imaging, a body that hurts, and nobody who could put it together. The odyssey to get pain explained turns out to be remarkably democratic.
Six months in, Los Angeles knows who we are. That is Irina.
Congratulations, and thank you. You bet on us, and we are very glad you did.
The free month is running, and the calendar is filling.
OxeFit assessments cost nothing for the rest of September — New Orleans and Beverly Hills both. Four days in, both cities are booking faster than we planned for.
If you have been meaning to do this, this is the week to get on the calendar rather than the week to think about it. There are a fixed number of assessment slots in a month and they do not carry over into October.
Most people have no objective idea how their body is performing. You know whether something hurts. You do not know whether your left side is quietly doing sixty percent of the work, whether your force production has dropped since last year, or where you are compensating in a way you cannot feel.
OxeFit puts that in numbers — how you produce and absorb force, strength, balance, side-to-side symmetry, movement quality — and turns it into a baseline you can act on and re-check later.
- Dancers and in-season athletes — symmetry and force data are exactly what you cannot get by feel, and feel is unreliable when you are tired.
- Hypermobility and connective-tissue patients — a stability and control baseline that is notoriously hard to capture any other way.
- Anyone coming back from injury — objective proof of where recovery actually stands, not just how it feels.
- Anyone over 40 — the earliest strength and balance changes are the ones worth catching.
Pick your city and take a slot — first come, first served.
September 1–30, 2026 · by appointment and subject to availability. An assessment is not a diagnosis and does not predict injury.
Beverly Hills
The Fascia Institute LA
Same assessment, same offer, on the West Coast.
Book Free OxeFit →The single-leg heel rise, and what your two sides tell you.
One minute, no equipment, and it measures something almost everyone is wrong about: whether your two legs are doing equal work.
How to do it. Stand facing a wall with your fingertips on it for balance only — not for support. Lift one foot off the floor. Rise onto the ball of the standing foot as high as you can, lower under control, and repeat at a steady pace of about one rise per second. Stop when your height noticeably drops, your heel stops clearing the same range, or you need the wall to hold you up. Write the number down. Rest a minute, then do the other side.
What you are looking for. Not the raw number — that varies enormously with age, sport, and training. Look at the difference between sides. Legs should be roughly comparable. When one side quits well before the other, you have found something worth a conversation. I want to be careful not to oversell it: the research linking movement asymmetry to future injury is genuinely inconsistent, and this test cannot predict anything. It is a prompt to look, not a forecast.
Dancers, this is the relevé you already do a hundred times a night, counted honestly and one leg at a time. Most people discover their push-off leg is not the strong one they assumed it was.
What it is not. Not a diagnosis, not a screening test, and not a reason to start training the weak side into the ground. Calf endurance is one input among many, and a low number can come from the foot, the ankle, the hip, the back, or simply from being tired today. Day-to-day variation on this test runs about six reps either way, so a small difference between sides is noise, not a finding. If a side difference is large, or if the test provokes pain, that is a reason to get looked at rather than a reason to grind.
Educational description of a movement test, not medical advice. Skip it if you have an acute injury, recent surgery, balance problems, or pain on weight-bearing. Do it near a wall. If you are hypermobile, stop well short of failure — repeated maximal single-leg work is a common way to subluxate an ankle or set off a flare. If you have POTS or orthostatic intolerance, do it seated-adjacent with someone nearby, or skip it.
Missed last week? Catch up on Vol. XIII — why your lumbar MRI probably is not the reason your back hurts, why hypermobility cannot be protocolized, and the episodes that get called seizures and are not.